scholarly journals Ingested interferon α suppresses Type I diabetes in non-obese diabetic mice

Diabetologia ◽  
1998 ◽  
Vol 41 (10) ◽  
pp. 1227-1232 ◽  
Author(s):  
S. A. Brod ◽  
M. Malone ◽  
S. Darcan ◽  
M. Papolla ◽  
L. Nelson
Keyword(s):  
Type I Diabetes ◽  
Interferon Α ◽  
Type I ◽  
Diabetic Mice

The Role of Interferon-α in the Development of Type I Diabetes

1996 ◽  
pp. 154-166
Author(s):  
Xiaojian Huang ◽  
Bruce Hultgren ◽  
Sharon Pitts-Meek ◽  
Jim Hully ◽  
Jim Maclachlan ◽  
...  
Keyword(s):  
Type I Diabetes ◽  
Interferon Α ◽  
Type I

scholarly journals Specific PKC βII inhibitor: one stone two birds in the treatment of diabetic foot ulcers

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Sushant Kumar Das ◽  
Yi Feng Yuan ◽  
Mao Quan Li
Keyword(s):  
Wound Healing ◽  
Protein Kinase ◽  
Peripheral Blood ◽  
Wound Closure ◽  
Type I Diabetes ◽  
Healing Process ◽  
Wound Healing Process ◽  
Peripheral Blood Flow ◽  
Type I ◽  
Diabetic Mice

To explore whether or not inhibition of protein kinase C βII (PKC βII) stimulates angiogenesis as well as prevents excessive NETosis in diabetics thus accelerating wound healing. Streptozotocin (STZ, 60 mg/kg/day for 5 days, i.p.) was injected to induce type I diabetes in male ICR mice. Mice were treated with ruboxistaurin (30 mg/kg/day, orally) for 14 consecutive days. Wound closure was evaluated by wound area and number of CD31-stained capillaries. Peripheral blood flow cytometry was done to evaluate number of circulating endothelial progenitor cells (EPCs). NETosis assay and wound tissue immunofluorescence imaging were done to evaluate the percentage of neutrophils undergoing NETosis. Furthermore, the expression of PKC βII, protein kinase B (Akt), endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF), and histone citrullation (H3Cit) were determined in the wound by Western blot analysis. Ruboxistaurin accelerated wound closure and stimulated angiogenesis in diabetic mice. The number of circulating EPCs was increased significantly in ruboxistaurin-treated diabetic mice. Moreover, ruboxistaurin treatment significantly decreases the percentages of H3Cit+ cells in both peripheral blood and wound areas. This prevented excess activated neutrophils forming an extracellular trap (NETs) formation. The expressions of phospho-Akt (p-Akt), phospho-eNOS (p-eNOS), and VEGF increased significantly in diabetic mice on ruboxistaurin treatment. The expressions of PKC βII and H3Cit+, on the other hand, decreased with ruboxistaurin treatment. The results of the present study suggest that ruboxistaurin by inhibiting PKC βII activation, reverses EPCs dysfunction as well as prevents exaggerated NETs formation in a diabetic mouse model; thereby accelerating the wound healing process.

scholarly journals Administration of Sulfatide to Ameliorate Type I Diabetes in Non-Obese Diabetic Mice

2014 ◽  
Vol 79 (4) ◽  
pp. 260-266 ◽  
Author(s):  
S. Rhost ◽  
L. Löfbom ◽  
J.-E. Månsson ◽  
A. Lehuen ◽  
M. Blomqvist ◽  
...  
Keyword(s):  
Type I Diabetes ◽  
Type I ◽  
Diabetic Mice

scholarly journals Contribution of Trem2 Signaling to the Development of Painful Diabetic Neuropathy by Mediating Microglial Polarization in Mice

2021 ◽  
Author(s):  
Xin Chen ◽  
Yue Le ◽  
Wan-you He ◽  
Jian He ◽  
Yun-hua Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Neuropathy ◽  
Mechanical Allodynia ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Thermal Hyperalgesia ◽  
Lumbar Spinal Cord ◽  
Type I ◽  
Painful Diabetic Neuropathy ◽  
Diabetic Mice

Abstract Background Painful diabetic neuropathy (PDN) is a common and intractable complication of diabetes mellitus, with little effective treatment. PDN has been associated with spinal neuroinflammation characterized by microglial activation. Recently, the triggering receptor expressed on myeloid cells 2 (TREM2), specifically localized on microglia, has been identified as a vital factor in modulating neuroinflammation and microglial phenotypes in neural diseases. Therefore, we hypothesized that spinal TREM2 might contribute to PDN and neuroinflammation by regulating microglial activity and phenotypes. Methods Type I diabetes mellitus was elicited by a single intraperitoneal administration of streptozotocin (STZ) in mice. The pain behaviors were reflected by paw mechanical withdrawal thresholds (PMWT) and thermal withdrawal latency (PTWL). Results We demonstrated that up-regulation of microglial TREM2 and amplification of both microglial M1 and M2 response was along with the presence of diabetes-related mechanical allodynia and thermal hypersensitivity. Moreover, we found that overexpression of TREM2 in microglia aggravated the symptom of PDN, amplified microglia M1 response, and suppressed microglia M2 polarization in the lumbar spinal cord of diabetic mice. However, inhibition of TREM2 with anti-TREM2 neutralizing antibodies attenuated mechanical allodynia and thermal hyperalgesia in diabetic mice. Besides, we identified Galectin-3 (GLT-3) as the potential ligand of the TREM2 receptor in facilitating the progression of PDN. Conclusions TREM2 could be a critical microglial membrane molecule that modulates microglial phenotypes pain hypersensitivity in PDN. GLT-3 might act as a specific ligand to trigger TREM2 signaling in PDN or other neuropathic pain.

scholarly journals In vivo antidiabetic activity of aqueous and ethyl acetate leaf extract of Senna singuena (Delile) in alloxan induced diabetic mice

2017 ◽  
Vol 6 (2) ◽  
pp. 84-92
Author(s):  
Njogu M. Stephen ◽  
◽  
Arika M. Wycliffe ◽  
Machocho K. Alex ◽  
Ngeranwa J.N. Joseph ◽  
...  
Keyword(s):  
Ethyl Acetate ◽  
Plant Extract ◽  
Leaf Extract ◽  
Type I Diabetes ◽  
Intraperitoneal Administration ◽  
Scientific Data ◽  
Hypoglycemic Activity ◽  
Antidiabetic Activity ◽  
Type I ◽  
Diabetic Mice

The folkloric claims that Senna singuena confers antidiabetic effect to prescribed patients has received long term clinical application accompanied by limited scientific data in support of such claims. This study aimed at bioscreening for hypoglycemic activity of the aqueous and organic fractions of S. singuena in alloxan induced diabetic mice. Type I diabetes mellitus was induced in mice by intraperitoneal administration of alloxan monohydrate followed by graded doses of the aqueous and ethyl acetate leaf extract administered to the experimentally diabetic mice following an overnight fast. The composition of the various phytochemicals of the plant extract was quantitatively assessed using standard procedures. Oral and intraperitoneal administration of the aqueous and ethyl acetate leaf extract caused a significant reduction in plasma glucose level in a dose independent manner in both fractions. The hypoglycemic activity could be attributed to phytoconstituents found in the plant extract. The generated data supports the folkloric claims associating S. singuena with hypoglycemic effects. However, there is need for further studies on this plant to investigate the mechanism of its activity and determine its safety profiles in order to explore possibilities of developing a new antidiabetic drug.

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